Endoplasmic reticulum stress induces Wfs1 gene expression in pancreatic beta-cells via transcriptional activation (Q24306636)

response to endoplasmic reticulum stress

GOA release 2020-03-11

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Wolframin ER transmembrane glycoprotein

GOA release 2020-03-11

1 reference

GOA release 2020-03-11

author name string

Kohei Ueda

1

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June Kawano

2

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Komei Takeda

3

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Toshiaki Yujiri

4

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Katsuya Tanabe

5

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Takatoshi Anno

6

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Masaru Akiyama

7

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Junichi Nozaki

8

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Takeo Yoshinaga

9

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Akio Koizumi

10

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Koh Shinoda

11

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Yoshitomo Oka

12

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Yukio Tanizawa

European Journal of Endocrinology

13

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language of work or name

English

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publication date

July 2005

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published in

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volume

153

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page(s)

167-76

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issue

1

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cites work

Reflexions on a newly discovered diabetogenic gene, wolframin (WFS1).

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Expression of estrogen receptors (alpha, beta) and androgen receptor in serotonin neurons of the rat and mouse dorsal raphe nuclei; sex and species differences

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A trip to the ER: coping with stress

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Neurodegeneration and diabetes: UK nationwide study of Wolfram (DIDMOAD) syndrome.

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The endoplasmic reticulum: integration of protein folding, quality control, signaling and degradation.

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Endoplasmic reticulum stress-mediated apoptosis in pancreatic beta-cells

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A gene encoding a transmembrane protein is mutated in patients with diabetes mellitus and optic atrophy (Wolfram syndrome)

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Identification and inhibition of the ICE/CED-3 protease necessary for mammalian apoptosis

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Identification of the cis-acting endoplasmic reticulum stress response element responsible for transcriptional induction of mammalian glucose-regulated proteins. Involvement of basic leucine zipper transcription factors

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Identification of ERSE-II, a new cis-acting element responsible for the ATF6-dependent mammalian unfolded protein response

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WFS1 (Wolfram syndrome 1) gene product: predominant subcellular localization to endoplasmic reticulum in cultured cells and neuronal expression in rat brain

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Diabetes insipidus, diabetes mellitus, optic atrophy and deafness (DIDMOAD) caused by mutations in a novel gene (wolframin) coding for a predicted transmembrane protein

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Wolfram syndrome: structural and functional analyses of mutant and wild-type wolframin, the WFS1 gene product.

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Disruption of the WFS1 gene in mice causes progressive beta-cell loss and impaired stimulus-secretion coupling in insulin secretion

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CHOP is implicated in programmed cell death in response to impaired function of the endoplasmic reticulum

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The endoplasmic reticulum stress response is stimulated through the continuous activation of transcription factors ATF6 and XBP1 in Ins2+/Akita pancreatic beta cells.

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ATF6 activated by proteolysis binds in the presence of NF-Y (CBF) directly to the cis-acting element responsible for the mammalian unfolded protein response

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Gadd153 sensitizes cells to endoplasmic reticulum stress by down-regulating Bcl2 and perturbing the cellular redox state

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Wolfram (DIDMOAD) syndrome.

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A mutation in the insulin 2 gene induces diabetes with severe pancreatic beta-cell dysfunction in the Mody mouse

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Establishment of a pancreatic beta cell line that retains glucose-inducible insulin secretion: special reference to expression of glucose transporter isoforms

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A novel locus, Mody4, distal to D7Mit189 on chromosome 7 determines early-onset NIDDM in nonobese C57BL/6 (Akita) mutant mice

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Genetically programmed selective islet beta-cell loss in diabetic subjects with Wolfram's syndrome

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Morbidity and mortality in the Wolfram syndrome

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